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1.
Cureus ; 11(7): e5203, 2019 Jul 22.
Artigo em Inglês | MEDLINE | ID: mdl-31565609

RESUMO

Wernicke encephalopathy is a neurological complication of thiamine deficiency, usually in the setting of poor diet, classically with alcoholism. Patients present with acute onset of encephalopathy, oculomotor dysfunction, gait ataxia and memory impairment. If untreated, the disorder can result in severe morbidity and possibly death; patient outcomes are entirely dependent on prompt diagnosis and administration of parenteral thiamine. Although diagnosed clinically, the radiologist may be able to alert the referring clinician to the possibility of the disease when imaging features are observed, thereby improving the chance of treatment success. Although various imaging features have been ascribed to alcohol and non-alcohol related forms of Wernicke encephalopathy, recent literature suggests that such a distinction is not reliable, and that the causes of Wernicke encephalopathy are not readily distinguishable on MRI, as in the index case presented here.

2.
Neuropharmacology ; 67: 95-103, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23159331

RESUMO

Methamphetamine induces monoamine depletions thought to contribute to cognitive and behavioral dysfunctions. Previously, we reported that methamphetamine-induced neurotoxicity is associated with impaired formation of stimulus-response associations. Additionally, subjective observations suggested that behavioral flexibility might be affected. Thus, the present study examined whether methamphetamine neurotoxicity induces perseverative behavior. Rats were pretreated with (±)-methamphetamine (4 × 10 mg/kg, 2-hr intervals) or saline. Three weeks later, rats were trained to press a lever on one side of an operant chamber and then retrieve the reinforcer from a magazine on the opposite side until they reached criterion (>50 reinforcers/30-min). After four consecutive sessions performing the task at criterion, rats were sacrificed and brains removed for monoamine determinations. Methamphetamine-pretreated rats had ∼50% loss of striatal dopamine and prefrontal serotonin. Methamphetamine- and saline-pretreated rats were not different in the number of sessions required to reach criterion or in the total numbers of lever presses and/or head entries made across the four consecutive sessions at criterion-level performance. However, methamphetamine-pretreated rats earned fewer reinforcers, because they made extra lever-presses and head entries when they should have been retrieving the reinforcer or returning to the lever. Latencies for methamphetamine-pretreated rats to switch between the two behaviors also were significantly slower than latencies for controls. Interestingly, the degree of additional lever-presses negatively correlated with serotonin-transporter binding in the prefrontal cortex, even in saline-pretreated controls. These data suggest that methamphetamine-induced partial monoamine toxicity is associated with perseveration and that the degree of perseveration may depend on serotonin innervation of the frontal cortex.


Assuntos
Condicionamento Operante/efeitos dos fármacos , Metanfetamina/toxicidade , Córtex Pré-Frontal/efeitos dos fármacos , Tempo de Reação/efeitos dos fármacos , Esquema de Reforço , Animais , Condicionamento Operante/fisiologia , Masculino , Córtex Pré-Frontal/metabolismo , Córtex Pré-Frontal/patologia , Ratos , Ratos Sprague-Dawley , Tempo de Reação/fisiologia , Serotonina/metabolismo
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